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© 2001 Nature Publishing Group http://medicine.nature.com
NEWS & VIEWS
Promiscuous regulator of xenobiotic removal
The transcription factor SXR mediates drug, xenobiotic and steroid induction of a major drug–metabolizing enzyme.
Drugs such as paclitaxel (Taxol) can bind and activate this transcription factor and therefore regulate their own
metabolism and efflux from cells. Manipulation of this pathway might lead to new ways to improve therapeutic
efficacy and to minimize toxicity (584-590).
enhanced clearance12. This indicates a
mental chemicals, endogenous broad role for SXR in the coordinated in
ERIN SCHUETZ1 & STEPHEN STROM2
T he body responds to drugs, environ
steroids and bile acids by inducing the co duction of multiple detoxification path
ordinated expression of a battery of drug some antileukemic agents, and such ther ways.
detoxification genes in tissues such as apy has been shown to exert negative ef Because concurrent administration of
liver and intestine. These include the cy fects on survival while increasing cancer CYP3A4 and P-glycoprotein inducers
tochromes P450 (CYPs), which are the relapse4 . Recent studies have shown that (such as rifampicin) with drugs that serve
enzymes responsible for oxidative, perox SXR, a member of the nuclear hormone as substrates for these proteins is a major
idative and reductive metabolism of toxic receptor superfamily, regulates expres basis of drug–drug interactions5 , pharma
compounds. Expression of drug transport sion of CYP3A (ref. 5,6). SXR is activated ceutical companies are now using SXR
proteins such as P-glycoprotein (encoded by a pharmacopia of drugs, including an binding and -activation assays to screen
by MDR1 and also known as MDR1 and tibiotics, statin cholesterol-lowering and predict which compounds will in
ABCB1) leads to the efficient efflux these drugs, antiseizure medications, steroids duce CYP3A expression and potentially
drugs from the body. Activation of drug such as glucocorticoids5 , some bile acids7 , cause drug interactions. These types of as
transport can be beneficial in instances environmental contaminants such as says may also identify compounds that
where it is important to remove toxins organochlorine pesticides and polychlori induce CYP2C9 and MDR1 , and cause
from the body, but detrimental in situa nated biphenyls8 , and herbal supple auto-induction of their own clearance. It
tions where it is important for a patient ments such as St. John’s wort9 . might be possible to someday create
to retain effective levels of a therapeutic Little is known about how certain drugs drugs that are ‘SXR transparent’ by mini
drug. In this issue, Snyold et al. 1 demon induce CYP and MDR1 gene expression. mizing or eliminating binding activity. In
strate that steroid xenobiotic receptor Synold et al. 1 demonstrate that SXR is ac this regard, the report of Synold et al . 1
(SXR; also known as PXR), a transcription tivated by paclitaxel (Taxol) and is re shows that docetaxel, unlike the struc
factor known to mediate drug, xenobiotic sponsible for inducing expression of not tural analog paclitaxel, does not induce
and steroid induction of the major liver only CYP3A (previously shown to be in CYP3A4 or MDR1 expression because it
drug metabolizing enzyme, can also regu duced by paclitaxel10) but also CYP2C9 does not activate SXR. This should result
late the expression of a drug efflux path and MDR1 . Paclitaxel is metabolized by in superior pharmacokinetic properties
©
way, indicating a novel strategy to both CYP3A4 and CYP2C9 (ref. 11) and relative to paclitaxel.
control drug clearance. transported by P-glycoprotein, and in Synold et al . 1 demonstrate that
CYP3A4, the most abundant drug-me duction of all of these proteins leads to its Ecteinascidin-743 (ET-743), an antineo
tabolizing enzyme in the liver and plastic agent, can antagonize SXR
intestine, is responsible for the activation and inhibit MDR1 ex
metabolism of 50% of all drugs. pression. The authors suggest that
Feed forward and feed back pathways
Many drugs are substrates for both SXR antagonists that downregu
CYP3A4 and P-glycoprotein, a late the P-glycoprotein pathway of
Paclitaxel
broad-specificity efflux pump pro drug elimination could be ex
tein encoded by the gene MDR1 . It ploited to improve drug retention.
was first demonstrated in 1996 This approach should be under
that MDR1 expression is coordi taken cautiously, because clinical
nated with expression of CYP3A4 , trials involving drugs that inhibit
with both gene products being in P-glycoprotein activity, given in an
SXR
duced by the same spectrum of effort to reduce drug resistance,
Regulates
drugs2 . P-glycoprotein and have had limited success and led to
the expression
CYP3A4 are colocalized in liver undesired pharmacokinetic side
of MDR1
and intestine, and serve as a coor effects13. MDR1 expression ‘modu
and CYP3A4
dinated system for the absorption, lators’ should be carefully screened
MDR1 CYP3A
CYP2C9
metabolism and disposition of for their potential to inhibit or
many drugs. Many drug–drug in modulate metabolism of other
teractions arise from concurrent medications taken by a patient.
Fig. 1 Feedforward and feedback pathways of drug metabo
administration of drugs which are Given the knowledge that SXR has
lism. Paclitaxel is a ligand for SXR, causing this nuclear receptor
both substrates and inducers of multiple detoxification genes as
to activate transcription of the P-glycoprotein efflux pump pro
CYP3A4 and MDR1 expression3 . targets, antagonism of SXR might
tein encoded by MDR1 , and the drug metabolizing enzymes
CYP3A and CYP2C9. These pathways, however, mediate drug
Long-term therapy with drugs lead to increased drug toxicity.
clearance and reduce paclitaxel activation of SXR in a feedback
that induce CYP3A4 and MDR1 in Synold et al . 1 emphasize the feed
mechanism. Manipulation of this pathway may be used to pro
crease the systemic clearance of forward pathways of drug clear
long or reduce drug retention.
536 NATURE MEDICINE • VOLUME 7 • NUMBER 5 • MAY 2001```
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